Identification and molecular cloning of <i>ncp1</i>.

<p>(A) Mutation in <i>NCP1</i> caused no-cotyledon phenotypes in seedling in <i>pid</i> background. From left to right, WT, <i>pid</i>, and <i>ncp1 pid</i>. (B) Adult plants of WT, <i>pid</i>, and <i>ncp1 pid</i>. (C) Electron micrographs of seedlings of WT (left), <i>pid</i> (middle), and <i>ncp1 pid</i> (right). Note that <i>ncp1 pid</i> failed to develop a cotyledon. (D) Late stage of embryos of WT, <i>pid</i>, and <i>ncp1 pid</i>. (E) Molecular cloning of <i>ncp1</i>. The mutation in <i>ncp1</i> was mapped to an interval of about 140 kb on Chromosome V. (F) A schematic gene structure of <i>At5g45550</i> and the location of T-DNA insertion of <i>ncp1-2</i>. Black boxes and lines designate exons and introns. The mutation at the splicing receptor of the second intron in <i>ncp1-1</i> led to a frame-shift and introduced a premature stop codon in cDNA. (G) Complementation of <i>ncp1-1</i> with a genomic DNA fragment of <i>At5g45550</i> gene. From left to right: WT and <i>ncp1 pid</i> with/without the <i>At5g45550</i> transgene (two seedlings of each). Note that the green transgenic seedlings had two or three cotyledons, while the yellowish non-transgenic seedlings had no cotyledon. The transformed <i>NCP1</i> gene restored <i>ncp1 pid</i> to <i>pid</i> phenotype. Scale bar, 2 mm (A), 5 cm (B), 100 μm (C), 25 μm (D), 1 mm (G).